NSG124 Pharmacology Study Test Plan Exam 3
Antihypertensives
• In patients with HF, aldosterone antagonists (e.g., spironolactone, eplerenone) reduce
symptoms and prolong life. Benefits derive from blocking aldosterone receptors in the
heart and blood vessels.
ACE Inhibitors: (-prils)
a. Mechanism:
i. ACE inhibitors block formation of angiotensin II, promote accumulation of
kinins, and reduce aldosterone release. As a result, these drugs cause
dilation of veins and arterioles, promote renal excretion of water, and
favorably alter cardiac remodeling.
1. By dilating arterioles, ACE inhibitors (1) improve regional
blood flow in the kidneys and other tissues and (2) reduce
cardiac afterload, which causes stroke volume and cardiac
output to rise.
2. By dilating veins, ACE inhibitors reduce venous pressure, which
in turn reduces pulmonary congestion, peripheral edema, preload,
and cardiac dilation.
3. By suppressing aldosterone release, ACE inhibitors increase
excretion of sodium and water, and decrease excretion of
potassium.
4. By increasing levels of kinins (and partly by decreasing levels of
angiotensin II), ACE inhibitors can favorably alter cardiac
remodeling
b. Therapeutic:
i. Hypertension, heart failure, MI left ventricular dysfunction and
nephropathy
c. Adverse effects:
i. First-dose hypotension, cough, angioedema, hyperkalemia (w/ potassium
supplements), renal failure (w/ renal stenosis), fetal injury
d. Patient education
i. Diuretics may increase first dose hypotension
ii. Potassium supplements and K sparking diuretics can cause hyperkalemia
iii. Monitor lithium
iv. NSAIDS may reduce affects
Angiotensin II Receptor Blockers: (-sartans)
e. Appropriate choice for pts who cannot tolerate ACE
f. Mechanism:
i. block access of angiotensin II to its receptors in blood vessels (causing
dilation), the adrenals (lowers aldosterone and increase water loss), and all
other tissues
g. Therapeutic:
i. Hypertension, heart failure, MI, stroke prevention and nephropathy
h. Adverse effects:
i. Less cough, less angioedema, less hyperkalemia, renal failure (w/ renal
stenosis), fetal injury
i. Patient education
i. Do not take with other hypertensive drugs
,• ARBs share the beneficial hemodynamic effects of ACE inhibitors, but not the
beneficial effects on cardiac remodeling.
a. In patients with HF, ARBs should be reserved for patients intolerant of ACE
inhibitors (usually owing to cough).
Aldosterone antagonists: (eplerenone and spironolactone)
b. Mechanism:
i. block receptors for aldosterone
c. Therapeutic:
i. hypertension and heart failure
• Patient education
o avoid potassium supplements and potassium-containing salt substitutes unless they
are prescribed by the provider. Potassium-sparing diuretics must also be avoided.
▪ Signs of high potassium – 3.5-5.0 – muscle spasm
o possibility of persistent dry, irritating, nonproductive cough with ACEs and ARBs
o do not use during pregnancy
o seek immediate medical attention if angioedema develops
o neutropenia: early signs of infection (fever, sore throat, mouth sores)
o minimize NSAID use
• Nursing interventions
o Stop diuretics
o avoiding potassium supplements and potassium-sparing diuretics except when they
are clearly indicated
o Monitor lithium levels frequently
• Nursing considerations
o ACEs and ARBs taken without regard to meal
o Aliskiren should be taken same time each day at mealtime
Calcium Channel Blockers – Verapamil and Nifedipine
• nifedipine and the other dihydropyridines act primarily on vascular smooth muscle
• verapamil and diltiazem act on vascular smooth muscle and on the heart
Verapamil:
o Mechanism: vasodilation accompanied by reduced arterial pressure and increased
coronary perfusion
o Therapeutic: angina (for vasodilation), hypertension (by dilating arterioles), cardiac
dysrhythmias (suppressing impulse conduction through the AV node)
o Adverse effects:
▪ constipation from blockade calcium channels in smooth muscle of intestine,
dizziness, facial flushing, headache, and edema of the ankles and feet from
vasodilation
▪ can cause bradycardia, partial or complete AV block
▪ gingival hyperplasia
o Patient education
▪ No grapefruit juice
▪ Inform patients about signs of edema (swelling in ankles or feet), and
instruct them to notify the prescriber if these occur
▪ Advise patients that constipation can be minimized by increasing dietary
, fluid and fiber
▪ Because they cause vasodilation, all CCBs can cause dizziness, headache,
and peripheral edema.
o Nursing Interventions
▪ Toxicity: overdose can produce severe hypotension and cardiotoxicity –
use activated charcoal, norepinephrine for hypotension and atropine for
bradycardia and heart block
o Nursing Considerations
▪ determine blood pressure and pulse rate, and obtain laboratory evaluations
of liver and kidney function
▪ contraindicated for patients with severe hypotension, sick sinus syndrom
Antihypertensives
• In patients with HF, aldosterone antagonists (e.g., spironolactone, eplerenone) reduce
symptoms and prolong life. Benefits derive from blocking aldosterone receptors in the
heart and blood vessels.
ACE Inhibitors: (-prils)
a. Mechanism:
i. ACE inhibitors block formation of angiotensin II, promote accumulation of
kinins, and reduce aldosterone release. As a result, these drugs cause
dilation of veins and arterioles, promote renal excretion of water, and
favorably alter cardiac remodeling.
1. By dilating arterioles, ACE inhibitors (1) improve regional
blood flow in the kidneys and other tissues and (2) reduce
cardiac afterload, which causes stroke volume and cardiac
output to rise.
2. By dilating veins, ACE inhibitors reduce venous pressure, which
in turn reduces pulmonary congestion, peripheral edema, preload,
and cardiac dilation.
3. By suppressing aldosterone release, ACE inhibitors increase
excretion of sodium and water, and decrease excretion of
potassium.
4. By increasing levels of kinins (and partly by decreasing levels of
angiotensin II), ACE inhibitors can favorably alter cardiac
remodeling
b. Therapeutic:
i. Hypertension, heart failure, MI left ventricular dysfunction and
nephropathy
c. Adverse effects:
i. First-dose hypotension, cough, angioedema, hyperkalemia (w/ potassium
supplements), renal failure (w/ renal stenosis), fetal injury
d. Patient education
i. Diuretics may increase first dose hypotension
ii. Potassium supplements and K sparking diuretics can cause hyperkalemia
iii. Monitor lithium
iv. NSAIDS may reduce affects
Angiotensin II Receptor Blockers: (-sartans)
e. Appropriate choice for pts who cannot tolerate ACE
f. Mechanism:
i. block access of angiotensin II to its receptors in blood vessels (causing
dilation), the adrenals (lowers aldosterone and increase water loss), and all
other tissues
g. Therapeutic:
i. Hypertension, heart failure, MI, stroke prevention and nephropathy
h. Adverse effects:
i. Less cough, less angioedema, less hyperkalemia, renal failure (w/ renal
stenosis), fetal injury
i. Patient education
i. Do not take with other hypertensive drugs
,• ARBs share the beneficial hemodynamic effects of ACE inhibitors, but not the
beneficial effects on cardiac remodeling.
a. In patients with HF, ARBs should be reserved for patients intolerant of ACE
inhibitors (usually owing to cough).
Aldosterone antagonists: (eplerenone and spironolactone)
b. Mechanism:
i. block receptors for aldosterone
c. Therapeutic:
i. hypertension and heart failure
• Patient education
o avoid potassium supplements and potassium-containing salt substitutes unless they
are prescribed by the provider. Potassium-sparing diuretics must also be avoided.
▪ Signs of high potassium – 3.5-5.0 – muscle spasm
o possibility of persistent dry, irritating, nonproductive cough with ACEs and ARBs
o do not use during pregnancy
o seek immediate medical attention if angioedema develops
o neutropenia: early signs of infection (fever, sore throat, mouth sores)
o minimize NSAID use
• Nursing interventions
o Stop diuretics
o avoiding potassium supplements and potassium-sparing diuretics except when they
are clearly indicated
o Monitor lithium levels frequently
• Nursing considerations
o ACEs and ARBs taken without regard to meal
o Aliskiren should be taken same time each day at mealtime
Calcium Channel Blockers – Verapamil and Nifedipine
• nifedipine and the other dihydropyridines act primarily on vascular smooth muscle
• verapamil and diltiazem act on vascular smooth muscle and on the heart
Verapamil:
o Mechanism: vasodilation accompanied by reduced arterial pressure and increased
coronary perfusion
o Therapeutic: angina (for vasodilation), hypertension (by dilating arterioles), cardiac
dysrhythmias (suppressing impulse conduction through the AV node)
o Adverse effects:
▪ constipation from blockade calcium channels in smooth muscle of intestine,
dizziness, facial flushing, headache, and edema of the ankles and feet from
vasodilation
▪ can cause bradycardia, partial or complete AV block
▪ gingival hyperplasia
o Patient education
▪ No grapefruit juice
▪ Inform patients about signs of edema (swelling in ankles or feet), and
instruct them to notify the prescriber if these occur
▪ Advise patients that constipation can be minimized by increasing dietary
, fluid and fiber
▪ Because they cause vasodilation, all CCBs can cause dizziness, headache,
and peripheral edema.
o Nursing Interventions
▪ Toxicity: overdose can produce severe hypotension and cardiotoxicity –
use activated charcoal, norepinephrine for hypotension and atropine for
bradycardia and heart block
o Nursing Considerations
▪ determine blood pressure and pulse rate, and obtain laboratory evaluations
of liver and kidney function
▪ contraindicated for patients with severe hypotension, sick sinus syndrom
